The prevalence of myopia (short sightedness) is increasing rapidly. Studies, for example, have shown a dramatic rise in the incidence of myopia (−0.25 D or more) in 7 year old Taiwanese children, from 4% to 16% between 1986 and 2000, and the prevalence of myopia (−0.25 D or more) in Taiwanese school children aged 16 to 18 years is as high as 84%. A population-based study in Mainland China reports that 55% of girls and 37% of boys at the age of 15 have significant myopia (−1.00 D or more).
Studies show that 50% of people with high myopia (over −6.00 D) have some form of retinal pathology. Myopia significantly increases the risk of retinal detachment, (depending on the level of myopia), posterior cataract and glaucoma. The optical, visual and potential pathological effects of myopia and its consequent inconvenience and cost to the individual and community, makes it desirable to have effective strategies to slow the progress, or prevent or delay the onset of myopia, or limit the amount of myopia occurring in both children and young adults.
Thus, a large percentage of the world's population has myopia at a level that requires some form of optical correction in order to see clearly. It is known that myopia, regardless of age of onset, tends to increase in amount requiring stronger and stronger correction. These corrections are available through a wide range of devices including spectacles, contact lenses and refractive surgery. These corrections, however, do little if anything to slow or stop the progression of myopia and arguably, according to some research findings, actually promote the progression of myopia.
One form of myopia, (often called “congenital myopia”), occurs at birth, is usually of high level, and may become progressively worse. A second type (sometimes called “juvenile myopia” or “school myopia”) begins in children at age 5 to 10 years and progresses through to adulthood or sometimes beyond. A third ‘type’ of myopia (which may be referred to as “adult myopia”) begins in young adulthood or late teenage years (16 to 19 years of age) and increases during adulthood, sometimes leveling off and at other times continuing to increase.
Strategies to prevent or slow myopia have been suggested that involve pharmacological interventions with anti-muscarinic drugs such as atropine (that are usually used to paralyze accommodation), or pirenzepine. However, the potential disadvantages associated with the long-term use of such pharmacological substances may render such modalities problematical.
It is known that during early development, the two eyes typically grow in a highly coordinated manner toward the ideal optical state, a process referred to as “emmetropization”. From the standpoint of optical intervention to prevent the onset, or retard the progression of myopia, three fundamental observations, which have been made in a variety of vertebrate animals ranging from birds to higher primates, have demonstrated conclusively that the emmetropization process is actively regulated by visual feedback.
First, conditions or experimental manipulations that prevent the formation of a clear retinal image cause the eye to grow abnormally long (called “axial elongation”) and to become myopic or short-sighted, a phenomenon referred to as “form-deprivation myopia”.
Second, if an eye that has form-deprivation myopia is subsequently allowed unrestricted vision, that eye then grows in a manner that eliminates the existing refractive error. This recovery requires visual feedback associated with the eye's effective refractive error because optically correcting the myopic error with spectacle lenses prevents recovery.
Third, imposing a refractive error on a normal eye (or “emmetropic” eye, one that is neither short-sighted nor long-sighted) with a spectacle lens produces compensating ocular growth that eliminates the refractive error produced by viewing through the lens, a phenomenon called “lens compensation”. Either myopia or hypermetropia (long-sightedness) can be induced in a variety of animal models including higher primates by the wearing of negatively-powered or positively-powered spectacle lenses, respectively. For example, when the image is positioned by the use of negative-powered lens to a position posterior to (i.e. behind) the retina, for example, myopia is induced. This myopia progression is actuated by axial elongation (growth bringing about a ‘lengthening’ of the eye-ball).
Thus, the mechanisms that are responsible for emmetropization monitor the retinal image and adjust axial growth rates to eliminate refractive errors. That is, the eye uses optical defocus to guide eye growth toward the ideal optical state.
For reasons that are not entirely understood, the emmetropization process goes awry in some individuals resulting in common refractive errors like myopia. Research using animal models strongly suggests that optical defocus could play a role in this process. Yet, to date treatment strategies for myopia that have manipulated the effective focus of the eye for central vision (e.g., bifocals) have had only limited success in preventing myopia or slowing down the progression of myopia.
For example, bifocal or progressive spectacle lenses or bifocal contact lenses have long been regarded as potential strategies for retarding the progress of myopia. However, studies on their efficacy show only limited efficacy. In the case of spectacle bifocals, compliance of the wearer to always look through the near addition portion for near work cannot be guaranteed. The bifocal contact lenses that have been used to date have been simultaneous vision bifocals. Such bifocals degrade the overall retinal image quality and are known to produce visual problems such as haloes, glare and ghosting, making them undesirable for the wearers.
Additional studies have shown that interrupting myopia-inducing stimuli, for even relatively short periods of time, reduces or even eliminates the myopia-inducing effects of such stimuli. The implication is that a ‘daily-wear’ approach, whereby the myope ceases to use the myopia-reduction device for certain periods during the day (e.g. removal after work and before sleep), would not be efficient and may well compromise its efficacy.
Another optical method, used in attempts to retard the progression of myopia in individuals is “under-correction”. In under-correction, the wearer is prescribed and provided with a correction (e.g. spectacles, or contact lenses) that is lower in amount than the full refractive prescription required for clear vision. For example, a −4.00 D myope may be given only a −3.50 D pair of spectacles rendering this myope still −0.50 D relatively myopic. Therefore, this method implicitly requires the central foveal visual image (the most important area for critical vision, e.g. visual acuity) to be blurred or degraded in some way. This significantly detracts from the usefulness of the device as the wearer is constantly reduced in visual performance, (e.g. preventing the wearer from driving due to legal vision requirements). Further, there is evidence to suggest that an under-correction approach may even accelerate myopia progression in some individuals.
A means of abating, retarding, and ultimately reversing, the progression of myopia, would provide enormous benefits to the millions of people who suffer from myopia as well as reduce the cost to individuals, health care workers and providers, and governments associated with myopia.